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Regulation of the co-evolved HrpR and HrpS AAA+ proteins required for Pseudomonas syringae pathogenicity

Milija Jovanovic, Ellen H. James, Patricia C. Burrows, Fabiane G. M. Rego, Martin Buck () and Jörg Schumacher ()
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Milija Jovanovic: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London
Ellen H. James: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London
Patricia C. Burrows: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London
Fabiane G. M. Rego: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London
Martin Buck: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London
Jörg Schumacher: Faculty of Natural Sciences, Sir Alexander Fleming Building, Imperial College London

Nature Communications, 2011, vol. 2, issue 1, 1-9

Abstract: Abstract The bacterial AAA+ enhancer-binding proteins (EBPs) HrpR and HrpS (HrpRS) of Pseudomonas syringae (Ps) activate σ54-dependent transcription at the hrpL promoter; triggering type-three secretion system-mediated pathogenicity. In contrast with singly acting EBPs, the evolution of the strictly co-operative HrpRS pair raises questions of potential benefits and mechanistic differences this transcription control system offers. Here, we show distinct properties of HrpR and HrpS variants, indicating functional specialization of these non-redundant, tandemly arranged paralogues. Activities of HrpR, HrpS and their control proteins HrpV and HrpG from Ps pv. tomato DC3000 in vitro establish that HrpRS forms a transcriptionally active hetero-hexamer, that there is a direct negative regulatory role for HrpV through specific binding to HrpS and that HrpG suppresses HrpV. The distinct HrpR and HrpS functionalities suggest how partial paralogue degeneration has potentially led to a novel control mechanism for EBPs and indicate subunit-specific roles for EBPs in σ54-RNA polymerase activation.

Date: 2011
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1177

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DOI: 10.1038/ncomms1177

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